Retinoblastoma protein-interacting zinc finger 1 (RIZ1) participates in RANKL-induced osteoclast formation via regulation of NFATc1 expression

Abstract

The role of retinoblastoma protein-interacting zinc finger 1 (RIZ1) in receptor activator of NF-κB ligand (RANKL)-induced osteoclast formation was examined in mouse RAW 264.7 macrophage-like cells. The expression of RIZ1 was significantly augmented by RANKL-treated cells. Silencing of RIZ1 with the siRNA significantly reduced the appearance of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells as osteoclasts in RANKL-treated cells. The expression of nuclear factor of activated T cell 1 (NFATc1) as the terminal transcription factor of osteoclast formation was prevented by RIZ1 siRNA. It was suggested that that RIZ1 might participate in RANKL-induced osteoclast formation through the regulation of NFATc1 expression.